Similarly, miR‐34a alone had little or no effect on tumor formation in mice.(37) It accelerated initiation and formation of tumors only when these mice were bred with other mice harboring oncogenic variant such as KrasG12D (Kras‐driven lung cancer model) or APC (colon cancer mouse model).(37, 38) Together, these loss‐of‐function mouse models suggest that the miR‐34 family is largely dispensable for p53 function and although not sufficient to initiate tumorigenesis, it may serve as an essential progression factor. This evidence concerns the gene KRAS and colonic neoplasm.